Abstract

Plant cells have multiple plasma membrane (PM)-localized calcium ATPases (ACAs) pumping calcium ions out of the cytosol. Although the involvement of some of these ACAs in plant growth and immunity has been reported, their individual and combined functions have not been fully examined. Here, we analysed the effects of single and combined mutations of four ACA genes, ACA8, ACA10, ACA12, and ACA13, in a number of processes. We found that these four genes had both overlapping and differential involvements in vegetative growth, inflorescence growth, seeds setting, disease resistance and stomatal movement. Disruption of any of these four genes reduces seed setting, indicating their contribution to the overall fitness of the plants. While ACA10 and ACA8 play major roles in vegetative growth and immunity, ACA13 and ACA12 are also involved in these processes especially when the function of ACA10 and/or ACA8 is compromised. The loss of ACA13 and ACA10 function in combination with a reduction in function of ACA8 leads to seedling death at bolting, revealing the essential role of their collective function in plant growth. Taken together, this study indicates a highly tuned calcium system involving these PM-localized calcium pumps in plant growth and environmental responses.

Highlights

  • Calcium (Ca2+) is an essential second messenger for cellular signal transduction and has a wide range of physiological roles in response to various environmental stimuli such as light, temperature, and pathogens (Sanders et al, 2002; McAinsh and Pittman, 2009; Dodd et al, 2010; Kudla et al, 2010)

  • ACA12 and ACA13 are the only two members in cluster 3, which is most closely related with cluster 4 that consists of plasma membrane (PM)-localized ACA8, ACA9, and ACA10 (George et al, 2008; Iwano et al, 2014) (Fig. 1A)

  • ACA12 was highly induced by these pathogens or pathogen signals except for Erysiphe orontii, with the highest fold induction among the four genes, while no induction was seen for ACA13 except in response; to Pseudomonas syringae (Supplementary Table S2B).The expression of these four genes did not seem to be responsive to many abiotic stresses, except that ACA8 was induced by cold, ACA10 and ACA12 were induced by UV-B, and ACA13 was induced by osmotic stress (Supplementary Table S2C)

Read more

Summary

Introduction

Calcium (Ca2+) is an essential second messenger for cellular signal transduction and has a wide range of physiological roles in response to various environmental stimuli such as light, temperature, and pathogens (Sanders et al, 2002; McAinsh and Pittman, 2009; Dodd et al, 2010; Kudla et al, 2010). It has been hypothesized that calcium carries information on the stimulus through the amplitude, frequency, and duration of calcium spikes (Dodd et al, 2010; Bonza and De Michelis, 2011) This Ca2+ signature is shaped by the combination of activities of membrane transport proteins in Ca2+. Calcium influx is mediated by a number of ion channels such as Ca2+-permeable cyclic nucleotide-gated channels and voltage-gated channels (Kudla et al, 2010). These channels reside at the plasma membrane (PM), endoplasmic reticulum (ER), vacuole, or mitochondria and are thought to collectively contribute to the dynamics of calcium signals (Geisler et al, 2000a; Sze et al, 2000; Boursiac and Harper, 2007). Ca2+ efflux requires cotransport systems and energy-dependent Ca2+ pumps such as the ER-type Ca2+ATPases (ECAs) and the autoinhibited Ca2+-ATPases (ACAs)

Methods
Results
Conclusion

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.